MECHANISM OF REGULATION OF NV-KB

NV-KB的调节机制

• 批准号: 2416850
• 负责人: DAVID M ROTHWARF
• 金额: $ 3.22万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-02-02 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2416850
• 关键词: alleles; biological signal transduction; enzyme activity; gene induction /repression; genetic regulation; genetic transcription; molecular cloning; phosphorylation; protein kinase; site directed mutagenesis; transcription factor

Scientific Merit; The goal of the proposed studies is to elucidate the signalling mechanisms involved in the activation of the transcription factor NF-kB. NF-kB is an inducible factor that is held in an inactive state i the cytoplasm by the inhibitory protein IkB. Exposure of cells to appropriate stimuli results in rapid phosphorylation and subsequent degradation of IkB with a resulting translocation of NF-kB to the nucleus, where it is involved in activation of gene transcription. The candidate proposes to identify the protein kinase that is responsible for phosphorylating IkB and then to study the mechanism of activation of this kinase. As a longer term goal, he will attempt to trace the signal transduction pathways for NF-kB back to cell surface receptors.

科学价值；拟议研究的目标是阐明 参与转录激活的信号机制 核因子-kB。核因子-kB是一种诱导因子，存在于不活跃的 状态I通过抑制蛋白IkB进入细胞质。细胞暴露于 适当的刺激导致快速的磷酸化和随后的 IKB的降解导致核因子-kB移位到细胞核， 它参与了基因转录的激活。候选人 建议确定负责的蛋白激酶 将IKB磷酸化，进而研究其激活机制 激活剂。作为一个更长期的目标，他将试图追踪这个信号 核因子-kB回到细胞表面受体的转导途径。